title: Infliximab improves vascular stiffness in patients with rheumatoid arthritis.
abstract: OBJECTIVE
  Patients with rheumatoid arthritis (RA) have increased cardiovascular mortality. Tumour necrosis factor alpha (TNFalpha)-blocking therapy has been shown to reduce RA disease activity measures and joint damage progression. Some observational studies suggest that TNFalpha blockade reduces mortality and incidence of first cardiovascular events. The mechanisms contributing to these outcomes are unclear. This study assessed the effects of infliximab treatment on vascular stiffness and structure in patients with RA.
  
  
  METHODS
  A post hoc analysis of longitudinal data from a randomised placebo controlled study evaluated the effect of infliximab on vascular assessments. 26 patients received intravenous infliximab (3 mg/kg) at weeks 0, 2, 6 and every 8 weeks thereafter to week 54. Patients were followed up to 56 weeks of infliximab therapy with assessments of RA disease activity, cardiovascular risk factors, vascular stiffness (pulse wave velocity (PWV)), carotid intima media thickness (CIMT) and carotid artery plaque (CAP). Univariate analyses of changes over time by repeated measures analysis of variance (ANOVA) were followed by multivariate time-series regression analysis (TSRA) if changes were seen.
  
  
  RESULTS
  PWV was significantly lower (better) after 56 weeks of treatment with infliximab (ANOVA p<0.01, TSRA p<0.01). However, CIMT (ANOVA p = 0.50) and CAP (chi(2) = 4.13, p = 0.88) did not change over the study period. Multiple cardiovascular risk measures did not change with treatment and did not correlate with changes in measures of vascular structure.
  
  
  CONCLUSIONS
  Arterial stiffness improves with infliximab treatment in RA. This change may help explain the improved cardiovascular disease survival in patients with RA receiving TNFalpha-blocking therapy.
authors.affiliation: Guy's and St Thomas' Hospital, London, UK.
authors.forename: M
authors.initials: M
authors.lastname: Wong
authors.forename: S P
authors.initials: SP
authors.lastname: Oakley
authors.forename: L
authors.initials: L
authors.lastname: Young
authors.forename: B Y
authors.initials: BY
authors.lastname: Jiang
authors.forename: A
authors.initials: A
authors.lastname: Wierzbicki
authors.forename: G
authors.initials: G
authors.lastname: Panayi
authors.forename: P
authors.initials: P
authors.lastname: Chowienczyk
authors.forename: B
authors.initials: B
authors.lastname: Kirkham
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000494:pharmacology* / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D001783:Blood Flow Velocity / Q000187:drug effects; D002340:Carotid Artery Diseases / Q000209:etiology / Q000473:pathology; D017536:Carotid Artery, Common / Q000187:drug effects / Q000473:pathology; D004812:Epidemiologic Methods; D005260:Female; D006801:Humans; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab